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. 2016 Oct 13;12(10):e1005910. doi: 10.1371/journal.ppat.1005910

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© 2016 Philip et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Fig 8 — TLR stimulation activates signaling complexes that mediate NF-κB and MAPK activation, which is required for induction of inflammatory cytokine gene expression. TLR stimulation also has the potential to induce programmed necrosis via RIPK3, or apoptosis via activation of caspase-8. Cleaved caspase-8 homodimers mediate apoptosis, whereas caspase-8/cFLIP heterodimers normally protect TLR-stimulated cells from programmed necrosis. Our data support a model whereby the caspase-8/cFLIP heterodimer also plays an important role in mediating inflammatory cytokine gene expression.